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Choi, Jang Hyun
Lab of Diabetes and Metabolism Lab.
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dc.citation.endPage 469 -
dc.citation.number 2 -
dc.citation.startPage 458 -
dc.citation.title JOURNAL OF NEUROCHEMISTRY -
dc.citation.volume 99 -
dc.contributor.author Kim, Hyeon Soo -
dc.contributor.author Song, Minseok -
dc.contributor.author Yumkham, Sanatombi -
dc.contributor.author Choi, Jang Hyun -
dc.contributor.author Lee, Taehoon -
dc.contributor.author Kwon, Joseph -
dc.contributor.author Lee, Sung Jae -
dc.contributor.author Kim, Jong-In -
dc.contributor.author Lee, Kang-Woo -
dc.contributor.author Han, Pyung-Lim -
dc.contributor.author Shin, Seung Woo -
dc.contributor.author Baik, Ja-Hyun -
dc.contributor.author Kim, Yong Sik -
dc.contributor.author Ryu, Sung Ho -
dc.contributor.author Suh, Pann-Ghill -
dc.date.accessioned 2023-12-22T09:41:43Z -
dc.date.available 2023-12-22T09:41:43Z -
dc.date.created 2014-10-14 -
dc.date.issued 2006-10 -
dc.description.abstract Haloperidol, a dopamine D2 receptor blocker, is a classical neuroleptic drug that elicits extrapyramidal symptoms. Its metabolites include 3-(4-fluorobenzoyl) propionic acid (FBPA) and 4-(4-chlorophenyl)-4-piperidinol (CPHP). Until now, the biological significance of these metabolites has remained largely unknown. Here, we report that the administration of FBPA to mice effected a suppression of locomotor activity and induced catalepsy in a manner similar to that observed with haloperidol, whereas CPHP had no significant effects. Neither of these two metabolites, however, exhibited any ability to bind to the dopamine D2 receptor. FBPA blocked dopamine-induced extracellular signal-regulated kinase 1/2 phosphorylation, and it specifically affected mitogen-activated protein kinase kinase (MEK)1/2 activity in hippocampal HN33 cells. Moreover, FBPA was capable of direct interaction with MEK1/2, and inhibited its activity in vitro. We demonstrated the generation of haloperidol metabolites within haloperidol-treated cells by mass spectrometric analyses. Collectively, our results confirm the biological activity of FBPA, and provide initial clues as to the receptor-independent role of haloperidol. -
dc.identifier.bibliographicCitation JOURNAL OF NEUROCHEMISTRY, v.99, no.2, pp.458 - 469 -
dc.identifier.doi 10.1111/j.1471-4159.2006.04108.x -
dc.identifier.issn 0022-3042 -
dc.identifier.scopusid 2-s2.0-33749173664 -
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/11001 -
dc.identifier.url http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33749173664 -
dc.identifier.wosid 000240834200010 -
dc.language 영어 -
dc.publisher WILEY-BLACKWELL -
dc.title Identification of a new functional target of haloperidol metabolite: implications for a receptor-independent role of 3-(4-fluorobenzoyl) propionic acid -
dc.type Article -
dc.description.journalRegisteredClass scopus -
dc.subject.keywordAuthor antipsychotic drug -
dc.subject.keywordAuthor dopamine D2 receptor -
dc.subject.keywordAuthor haloperidol -
dc.subject.keywordAuthor metabolite -
dc.subject.keywordAuthor mitogen-activated protein kinase kinase -
dc.subject.keywordPlus ACTIVATED PROTEIN-KINASE -
dc.subject.keywordPlus PERFORMANCE LIQUID-CHROMATOGRAPHY -
dc.subject.keywordPlus PYRIDINIUM METABOLITE -
dc.subject.keywordPlus MASS-SPECTROMETRY -
dc.subject.keywordPlus SIGMA-RECEPTORS -
dc.subject.keywordPlus 2 ISOFORMS -
dc.subject.keywordPlus IN-VIVO -
dc.subject.keywordPlus STIMULATION -
dc.subject.keywordPlus DOPAMINE-D-2 -
dc.subject.keywordPlus CATALEPSY -

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